[miR-153 aggravates lung injury induced by lipopolysaccharide via inhibiting activated protein C (APC) in rats with sepsis and its mechanism].

作者：Yadong Yang, Jine Peng, Qiu-Fang She, Yu Tang, Jiang Wang, Jinpeng Zhang, Xing Liu, Rongsong Cai, Zirao Zhou, Shuang Zeng, Xu Ji · 发表于：PubMed · 年份：2022 · 被引用次数：1 · 研究领域：Inflammation biomarkers and pathways、Immune Response and Inflammation、Cell death mechanisms and regulation

Objective To investigate the mechanism of miR-153 targeting activated protein C (APC) to regulate lipopolysaccharide (LPS)-induced lung injury in rats with sepsis. Methods Female SD rats were divided into control group, LPS group, LPS combined with miR-153 inhibitor (miR-153 inhibitor) group, LPS combined with miR-153 inhibitor negative control (inhibitor NC) group, LPS and miR-153 inhibitor combined with APC small interfering RNA (si-APC) group, LPS and miR-153 inhibitor combined with APC small interfering RNA negative control (si-NC) group. Except for the control group, the other groups were given corresponding treatments, and then LPS were given to establish rat sepsis injury models. Real-time quantitative PCR was used to detect the expression of miR-153 and Western blot analysis to detect the protein expression of APC, B-cell lymphoma 2 (Bcl2) and cleaved caspase-3 (c-caspase-3). The rat alveolar epithelial cells were isolated and cultured, and their cell viability was detected by CCK-8 assay, along with cell apoptosis detected by flow cytometry. ELISA was performed to test the expression levels of superoxide dismutase (SOD), malondialdehyde (MDA), interleukin 6 (IL-6), IL-1β and tumor necrosis factor α (TNF-α) in rat serum; and the dual fluorescein reporter experiment detects the relationship between miR-153 and APC. Results Compared with the control group, rat model of sepsis lung injury showed significantly increased expression of miR-153 and reduced APC. The cell viab...